The primary aim of the program is the development of novel agents capable of counteracting the enhanced tendency for blood platelet adhesion, release and aggregation in persons (i) bearing prosthetic devices or (ii) linked to biomaterials in contact with their blood; the foremost concern being the prevention of thromboembolic complications. Since there is convincing evidence that acetylation capability and surface activity are factors of prominent significance in the action of antithrombotic compounds, we are seeking to optimize both of these parameters within the framework of single new molecules; the surface-active features are expected to markedly enhance interaction with acetylation-sensitive and other platelet target-sites, and possibly, with other pertinent biologic entities. The new synthetic compounds, conceived and designed based on the aforementioned premises, are evaluated inreference to the parent compound aspirin in terms of their ability (1) to inhibit human platelet retention by select biomaterial surfaces (e.g., Cuprophane; Silastic); (2) to inhibit human platelet aggregation induced by collagen, thrombin, adenosine diphosphate epinephrine, and arachidonic acid, (3) to accumulate at, and penetrate, interfaces as reflected by interfacial tension and partition coefficient measurements; and (4) to interact with components of platelet surface structures, or closely related entities, in monomolecular-film systems.